Tetanus: An Important Disease of Sheep and Goat

Tetanus: An Important Disease of Sheep and Goat

Siddiqui M.F.M.F.¹ A.K. Wankar² and S.R.³ Shaikh

Department of Veterinary Clinical Medicine, Ethics & Jurisprudence

College of Veterinary and Animal Sciences, MAFSU, Parbhani, India- 431 402

1 Assistant Professor, Department of Veterinary Clinical Medicine, Ethics & Jurisprudence College of Veterinary and Animal Sciences, MAFSU, Parbhani, Maharashtra, India -431 402. drmfmfsiddiqui@gmail.com, +91 9960147171 (Corresponding Author) (Reprint requests are solicited at this address)

2 Assistant Professor, Department of Veterinary Physiology, College of Veterinary and Animal Sciences, MAFSU, Parbhani, Maharashtra, India -431 402. (09860588149)

3 PhD Scholar, Department of Veterinary Clinical Medicine, Ethics & Jurisprudence, College of Veterinary and Animal Sciences, MAFSU, Parbhani, Maharashtra, India-431 402. salahuddinshkh@gmail.com; +91 8983195305

Abstract:

Tetanus is a non-contagious, non-febrile, infectious disease of mammals affected by exotoxins. It is characterized by spasmodic contractions of skeletal muscles and death in affected animals. Typically, tetanus is a toxemia caused by neurotoxin produced under anaerobic conditions by Clostridium tetani, a gram positive, spore-forming obligate anaerobe bacillus. Tetanus occurs in all parts of the world and is most common in closely settled areas under intensive cultivation. C. tetani organisms are commonly present in the faeces of sheep & goat and in the soil contaminated by these faeces. The portal of entry is usually through deep puncture wounds, but the spores may lie dormant in the tissues for some time and produce clinical illness only when tissue conditions favor their proliferation. For this reason, the portal of entry is often difficult to identify. Sheep and goat are relatively more resistant but most commonly occurs in lambs, kids and rarely occurs in adult animals. The tetanus spores remain localized at their site of introduction and spores germinate to their vegetative form to proliferate and produce tetanolysin, tetanospasmin and neurotoxin after anaerobic condition development. There are no gross or histologic findings by which a diagnosis can be confirmed but demonstrating the presence of tetanus toxin in serum from the affected animal may be suggestive of the Tetanus infection. Treatment involves four steps as eliminate the causative bacteria, neutralize residual toxin, control muscle spasms until the toxin is eliminated or destroyed, maintain hydration and nutrition and provide supportive treatment. Many cases of tetanus could be avoided by proper skin and instrument disinfection at castrating, docking and shearing time and on time vaccination. Proper and on time treatment can save the life of tetanus infected sheep and goat though recovery is uneven.

Keywords: Tetanus, toxoid, sheep, goat, Clostridium spp., toxin

INTRODUCTION:

Tetanus is a non-contagious, non-febrile, infectious disease of mammals affected by exotoxins. It is characterized by spasmodic contractions of skeletal muscles and death in affected animals. Typically, tetanus is a toxemia caused by neurotoxin produced under anaerobic conditions by Clostridium tetani. Bacillus Cl. tetani is a gram positive, rod shape, spore forming and anaerobic bacteria. This condition occurs in all farm animals, mainly as sporadic cases. The spore of the bacteria is found widely in both soil and animal faeces. Horses are highly sensitive to the disease, followed by sheep and goat, while dogs and cat are relatively resistant (Parmaret al., 2015). Most commonly occurs in young lambs, kids, calves and rarely occurs in adults (Dhanavelet al., 2018). Goats are very susceptible to the disease (Mohamad et al., 2013). Infection occurs as a result of contamination of wounds or enclosed cavities by the spores of C. tetani. In anaerobic conditions these spores covert to the vegetative forms, capable of life producing fetal toxins as tetanolysin, tetanospasmin and neurotoxin or nonspasmolytic toxin (Constable et al., 2017). The clinical signs usually appear 4-21 days after entry of organism. In goats, clinical signs include erect ears, elevated tail, extended and stiff neck, general muscle stiffness, saw horse posture, prolapse of third eye lid, dysphagia, lock jaw and hyperaesthesia. In later stages the animal goes to lateral recumbency and deaths results. In goats like other ruminants, constipation and tympany are very pronounced. Diagnosis is usually done on the basis of history, clinical findings and isolation and identification of Cl. tetani organism. It is possible to keep the animal alive by using tetanus antitoxin, a muscle relaxant, antibiotics and supportive drugs.

EPIDEMIOLOGY:

Etiology:

Tetanus is caused by C. tetani, a gram positive, spore-forming obligate anaerobe bacillus. It is a ubiquitous organism and a commensal of the gastrointestinal tract of domestic animals and humans. The organism forms highly resistant spores that can persist in soil for many years. The spores survive many standard disinfection procedures, including steam heat at 100°C (212°F) for 20 minutes but can be destroyed by heating at 115°C (239°F) for 20 minutes. After a period of anaerobic incubation spores germinate to their vegetative form, which starts replicating and producing a complex of exotoxins causing the clinic signs characteristic for this condition. The toxins produced are tetanolysin, tetanospasmin and neurotoxin or nonspasmolytic toxin (Constable et al., 2017).

Occurrence:

Tetanus occurs in all parts of the world and is most common in closely settled areas under intensive cultivation. It occurs in all farm animals, mainly as individual, sporadic cases, although outbreaks are occasionally observed in young sheep and goat following wound management procedures.

Source of Infection:

1. tetani organisms are commonly present in the faeces of sheep & goat and in the soil contaminated by these faeces. Surveys in different areas of the world show it is present in 30% to 42% of soil samples. The survival period of the organism in soil varies widely from soil to soil (Constable et al., 2017).

Transmission:

The portal of entry is usually through deep puncture wounds, but the spores may lie dormant in the tissues for some time and produce clinical illness only when tissue conditions favor their proliferation. For this reason, the portal of entry is often difficult to identify. A high incidence of tetanus may occur in lambs and kids following castration, shearing, docking, vaccinations or injections of pharmaceuticals, especially anthelmintics. Mohamad and Syed (2013) reported a case of tetanus suffering from horn fracture which was treated by farmer with a hot iron and rubbed some unsterile oils without using any disinfectant substances. Docking by the use of elastic band ligatures is reported to be especially hazardous. Another most common route is wound at different parts like chronic wound at carpal region (Parmar et al., 2015). Chandranaik et al. (2009) found that the soil contaminated with the spores entered into the wounds created by the ear tags was the cause of outbreak of tetanus in sheep.

Neonatal tetanus occurs when there is infection in the umbilical cord associated with unsanitary conditions at parturition. Cases of tetanus in ruminants after thermic dehorning and ear-tagging also have been reported.

Animal Risk Factors

The neurotoxin of C. tetani is exceedingly potent, but there is considerable variation in susceptibility between animal species but horses are the most susceptible. The variation in prevalence of the disease in the different species is partly caused by this variation in susceptibility but is also because exposure and wound management practices are more likely to occur in some species than in others. Sheep and goat are relatively more resistant than horses but less sensitive than dog and cat (Parmar et al., 2015). It occurs irrespective of sex of animals. Most commonly occurs in lambs, kids and rarely occurs in adult animals (Dhanavel, 2012).

PATHOGENESIS

The tetanus spores remain localized at their site of introduction and do not invade surrounding tissues. Spores germinate to their vegetative form to proliferate and produce tetanolysin, tetanospasmin and neurotoxin only if certain environmental conditions are attained, particularly a lowering of the local tissue oxygen tension (Constable et al., 2017). Toxin production may occur immediately after introduction if the accompanying trauma has been sufficiently severe or if foreign material has also been introduced to the wound or may be delayed for several months until subsequent trauma to the site causes tissue damage. Of the three mentioned exotoxins, tetanospasmin is the most relevant for the pathophysiology of the condition. Although tetanolysin was found to promote local tissue necrosis, its role in the pathogenesis of tetanus remains doubtful. The role of the more recently identified neurotoxin, or nonspasmogenic toxin, which is a peripherally active for the pathophysiology of tetanus, is currently unknown.

Tetanospasmin diffuses to the systemic circulation, is bound to motor end plates and travels up peripheral nerve trunks via retrograde intra-axonal transport to the CNS. The exact mechanisms by which the toxin exerts its effects on nervous tissue are not known, but it blocks the release of neurotransmitters such as GABA and glycine, which are essential for the synaptic inhibition of gamma motor neurons in the spinal cord (Kahn & Line, 2011). There it leads to an unmodulated spread of neural impulses produced by normally innocuous stimuli, causing exaggerated responses and a state of constant muscular spasticity. No structural lesions are produced. Death occurs by asphyxiation caused by fixation of the muscles of respiration.

CLINICAL FINDINGS

The incubation period varies between 3 days and 4 weeks, with occasional cases occurring as long as several months after the infection are introduced. In sheep and goat cases appear 3 to 10 days after shearing, docking or castration. Clinical findings are almost similar in both animals. Initially, there is an increase in muscle stiffness, accompanied by muscle tremor. There is trismus with restriction of jaw movement), prolapse of the third eyelidear erection,stiffness of the hindlimbs causing an unsteady, straddling gait; and the tail is held out stiffly, especially when backing or turning  (Dhanavel, 2012;Mohamad and Syed, 2013; Muralidharann et al., 2010).

Retraction of the eye and prolapse of the third eyelid (a rapid movement of the third eyelid across the cornea followed by a slow retraction) is one of the earliest and consistent signs (with the exception of sheep) and can be exaggerated by sharp lifting of the muzzle or tapping the face below the eye. Additional signs include an anxious and alert expression contributed to by an erect carriage of the ears, retraction of the eyelids and dilation of the nostrils and hyperesthesia with exaggerated responses to normal stimuli. The animal may continue to eat and drink in the early stages but mastication is soon prevented by tetany of the masseter muscles and saliva may drool from the mouth. If food or water is taken, attempts at swallowing are followed by regurgitation from the nose.

Constipation is usual and the urine is retained, partly as a result of the inability to assume the normal position for urination. The rectal temperature and pulse rate are within the normal range in the early stages but may rise later when muscular tone and activity are further increased. As the disease progresses, muscular tetany increases and the animal adopts a sawhorse posture. Uneven muscular contractions may cause the development of a curve in the spine and deviation of the tail to one side. There is great difficulty in walking and the animal is inclined to fall (Muralidharann et al., 2010). Falling occurs with the limbs still in a state of tetany and the animal can cause itself severe injury. Once down it is almost impossible to get a large animal to its feet again. Tetanic convulsions begin in which the tetany is still further exaggerated. Opisthotonus is marked, the hindlimbs are stuck out stiffly behind and the forelegs forward. Sweating may be profuse and the temperature rises, often to 42°C (107°F). Respiratory rate and heart rate are usually increase to 66 breaths per minutes and 110 beats per minutes respectively (Mohamad and Syed, 2013 and Muralidharann et al., 2010).

The convulsions are at first only stimulated by sound or touch but soon occur spontaneously. In fatal cases there is often a transient period of improvement for several hours before a final, severe tetanic spasm during which respiration is arrested. The course of the disease and the prognosis vary both between and within species. The duration of a fatal illness in sheep is usually third or fourth day (Constable et al., 2017). A long incubation period is usually associated with a mild syndrome, a long course and a favorable prognosis. Mild cases that recover usually so slowly, with the stiffness disappearing gradually over a period of weeks or even months. The prognosis is poor when signs rapidly progress.

CLINICAL PATHOLOGY:

Parmar et al., (2015) reported that leukocytosis with neutrophilia and other parameters viz. Hb, PCV, TEC, lymphocytes, monocytes, eosinophils and basophils in normal range. Blood levels of tetanus toxin are usually too low to be detected. Gramstain of wound aspirates is considered of limited value because sporulated as well as vegetative forms of C. tetani resemble other anaerobic bacteria. Culturing the pathogen is difficult because of the low number of organisms normally present and the strict anaerobic conditions required for culture.

Chandranaik et al. (2009) found lowered hameoglobin (4-6 gm%), milk neutrophilia and other parameters in normal rage. However, biochemical parameters in ailing animals showed deficiency of calcium (4.1 – 5.6 mg/dL) and phosphorus (3.2 – 5.1 mg/dL), altered liver and kidney (BUN, 65 mg/dL, Creatinine – 2.2) function test values which were suggestive of anaemia and debility due to inanition.

Culture in combination with PCR has been used for identification of C. tetani. A bioassay consisting of injecting infectious material into the tail base of mice and observing for onset of characteristic clinical signs is possible.

NECROPSY FINDINGS:

There are no gross or histologic findings by which a diagnosis can be confirmed, although a search should be made for the site of infection. Culture of the organism is difficult but should be attempted. If minimal autolysis has occurred by the time of necropsy, the identification of large gram-positive rods with terminal spores (“tennis-racket morphology”) in smears prepared from the wound site or spleen is supportive of a diagnosis of tetanus.  Muralidharn et al., (2010) and Chandranaik et al., (2009) reported emphysematous lungs and congestion of the vital organson post mortem of sheep having tetanus.

Diagnosis:

The clinical signs and history of recent trauma are usually adequate for a clinical diagnosis of tetanus. It may be possible to confirm the diagnosis by demonstrating the presence of tetanus toxin in serum from the affected animal. In cases in which the wound is apparent, demonstration of the bacterium in gram-stained smears and by anaerobic culture may be attempted (Kahn & Line, 2011). The samples used for confirmative diagnosis for bacteriological examination are air-dried impression smears from spleen, wound site (cyto,Gram stain), culture swab from wound site in anaerobic transport media; spleen in sterile, leak-proof container (anaerobic CULT, bioassay) (Constable et al., 2017).

TREATMENT:

These are the main principles in the treatment of tetanus (Constable et al., 2017):

1. Eliminate the causative bacteria
2. Neutralize residual toxin
3. Control muscle spasms until the toxin is eliminated or destroyed
4. Maintain hydration and nutrition
5. Provide supportive treatment

There are no structural changes in the nervous system and the management of cases of tetanus depends largely on keeping the animal alive through the critical stages.

• Eliminate the causative bacteria:

Elimination of the organism is usually attempted by the parenteral administration of penicillin in large doses – 20, 000 to 44,000 IU/kg body weight (Muralidharann et al., 2010), preferably by intravenous administration. Other antimicrobials that have been proposed include oxytetracycline (15 mg/kg body weight), macrolides and metronidazole.

• Neutralize residual toxin

If the infection site is found, the wound should be aggressively cleaned and debrided but only after antitoxin has been administered, because debridement, irrigation with hydrogen peroxide and the local application of penicillin may facilitate the absorption of the toxin. The objective of administering tetanus antitoxin is to neutralize circulating toxin outside the CNS. The use of tetanus antitoxin is most appropriate in wounded animals that are susceptible to but unvaccinated against tetanus or with uncertain vaccination history. Because binding of tetanospasmin to neural cells is irreversible and because the tetanus antitoxin is unable to penetrate the blood brain barrier, administration of antitoxin is of little value once signs have appeared.

After the experimental administration of toxin, antitoxin is of limited value at 10 hours and ineffective by 48 hours. The recommended doses vary widely and range from 10,000 to over 300,000 IU per treatment, given intravenously, intramuscularly, or subcutaneously once or repeatedly, but reported treatment outcomes are inconsistent. Local injection of some of the antitoxin around the wound has also been proposed. There have been anumber of attempts to justify the treatmentof early cases of equine tetanus by intrathecal injection of antitoxin, but there is limited evidence of therapeutic value and the procedure carries risk.

The use of tetanus toxoid has also been recommended for patients with tetanus, but an antibody response may take 2 to 4 weeks and a booster vaccination is required in previously unvaccinated animals. The effectiveness of this treatment in previously unvaccinated animals is therefore doubtful. When combining tetanus toxoid and antitoxin, both compounds should be administered on different sites using different syringes.

• Control muscle spasms until the toxin is eliminated or destroyed:

Relaxation of the muscle tetany can be attempted with various drugs. Chlorpromazine @ 0.4–0.8 mg/kg BW intravenously, or 1.0 mg/kg BW intramuscularly, three or four times daily (Muralidharann et al., 2010) and acepromazine @ 0.05 mg/kg BW three to four times daily administered until severe signs subside (Mohamad & Syed, 2013).

• Maintain hydration and nutrition:

Hydration can be maintained by intravenous or stomach tube feeding during the critical stages when the animal cannot eat or drink. The use of an indwelling tube should be considered because of the disturbance caused each time the stomach tube is passed. Feed and water containers should be elevated and the feed should be soft and moist.

• Provide supportive treatment:

Affected animals should be kept as quiet as possible and provided with dark, well bedded quarters with nonslip flooring and plenty of room to avoid injury if convulsions occur. Administration of enemas and catheterization may relieve the animal’s discomfort.

This level of nursing, plus penicillin, ataractic drugs and antitoxin for an average of 14 days, can deliver something like a 50%recovery by an average of 27 days, but the cost is high. A rumenostomy may be required in tetanic animal with recurrent bloat.

In a field trial conducted by Umadevi et al. (2016) four goats and two sheep having tetanus were treated with locally distilled alcohol five to ten ml or 20-50 ml of banded alcohol twice daily for 20 days. Animas were given forceful liquid feeding and stabled.

CONTROL

Many cases of tetanus could be avoided by proper skin and instrument disinfection at castrating, docking and shearing time. These operations should be performed in clean surroundings; in the case of lambs docked in the field, temporary pens are preferred over permanent yards for catching and penning.

Passive Immunity

Short-term prophylaxis can be achieved by the injection of 1500 IU of tetanus antitoxin. The immunity is transient, persisting for only 10 to 14 days.

Tetanus Antitoxin

Tetanus antitoxin should be given to any horse with a penetrating wound or deep laceration, and the wound should also be cleaned aggressively. Tetanus toxoid can be administered at the same time as tetanus antitoxin, provided they are injected at different sites and using different syringes. Animals that suffer injury are usually given an injection of antitoxin and one of toxoid to ensure complete protection. On farms where the incidence of tetanus in lambs is high, antitoxin is usually given at the time of docking or castration; 200 IU has been shown to be effective (Constable et al., 2017 and Kahn and Line, 2011). The risk for tetanus in calves is lower than in lambs and tetanus antitoxin is not commonly given at the time of castration.

Active Immunity:

Available vaccines are formalin-inactivated adjuvanted toxoids; they induce long-lasting immunity. Primary vaccination requires two doses 3 to 6 weeks apart. Protective titers are obtained within 14 days of the second injection and last for at least a year and up to 5years.Ewes are immunized with a similar schedule except that the primary doses are usually given at a managemental convenient time when the flock is yarded (Constable et al., 2017). A pre-lambing booster vaccination is given yearly. Commonly, commercial vaccines for sheep also contain antigens for other clostridial diseases for which sheep are at high risk.

Recovery:

Generally complete recovery requires 7 to 15 days (Dhanavel, 2012). When the proper treatment is given on time with adequate comfort to animal recovery can be occur. Tetanus anti-toxin is not usually effective once the toxin has reached the spinal cord, injecting it immediately is vital if the goat is to have any chance of surviving (Mohamad & Syed, 2013). Tetanus affected goats and sheep were treated with locally distilled (or) branded alcohol and found 99% recovered from 25 days of treatment (Umadevi et al., 2016). Death may occur due to uncontrollable muscle spasms of diaphragm and inter-costals muscles leading to respiratory failure (Muralidharann et al., 2010) while Chandranaik et al. (2009) observed recovery in about 25% of the sheep only.

Conclusion:

In short, small ruminants like sheep and goats are comparatively resistant to tetanus infection than large ruminants. Negligence, unhygienic and septic conditions during surgical operations like castrating, docking and shearing time and not on time and improper vaccination are the main causes of tetanus. Proper and on time treatment can save the life of tetanus infected sheep and goat though recovery is uneven.

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Successful Treatment of Tetanus in a ND Goat – a case report